Jie Fan

Fax: 412-688-6204

1W142 VAMC

Professor of Surgery, Director of the Multidisciplinary Surgery Research Program at VA Pittsburgh Healthcare System


M.S - Second Military Medical University

M.D. - Shanghai Second Medical University.

Ph.D. - State University of New York at Stony Brook

Research Summary

Dr. Fan has long been focusing on cellular and molecular mechanisms of cell priming in sepsis and organ injury after hemorrhagic shock. His team has explored a number of novel mechanisms of receptor crosstalk and cell-cell interaction underlying post-shock systemic inflammation and lung injury, and has been featured in numerous publications. The ongoing research projects in Dr. Fan’s lab include several lines that aim to elucidate the mechanisms of hemorrhagic shock-induced activation of inflammasome, pyroptosome, and autophagy in innate immune cells, as well as the significances of the resultant alterations in the development of post-hemorrhage systemic inflammatory response syndrome.

Lab Affiliation

Lab Role



(Selected from more than 80 publications)

Xu J, Jiang Y, Wang J, Shi X, Liu Q, Liu Z, Li Y, Scott MJ, Xiao G, Li S, Fan L, Billiar TR, Wilson MA, and Fan J. Macrophage Endocytosis of High Mobility Group Box 1 Triggers Pyroptosis. Cell Death and Differentiation 2014.4 (Advance online publication)

Xu P, Wen Z, Shi X, Li Y, Fan L, Xiang M, Li A, Scott M J, Xiao G, Li S, Billiar TR, Wilson MA, and Fan J. Hemorrhagic Shock Augments Nlrp3 Inflammasome Activation in the Lung through Impaired Pyrin Induction. J Immunol. 2013, 190(10):5247.

Liu Z, Jiang Y, Li Y, Wang J, Fan L, Scott MJ, Xiao G, Li S, Billiar TR, Wilson MA, and Fan J.  TLR4 Signaling Augments Monocyte Chemotaxis by Regulating G ProteinCoupled Receptor Kinase 2 Translocation. J. Immunol. 2013, 191 (2): 857.

Xiang M, Shi X, Li Y, Xu J, Yin L, Xiao G, Scott MJ, Billiar TR, Wilson MA, Fan J. Hemorrhagic Shock Activation of NLRP3 Inflammasome in Lung Endothelial Cells. J Immunol.  2011, 187:4809-4817.

Fan J and Malik AB. Toll-like receptor 4 signaling augments chemokine-induced neutrophil migration by modulating cell surface expression of chemokine receptors. Nature Medicine 2003, 9(3): 315.